Hepatic Artery Thrombosis

Vascular complications are a major source of morbidity and graft loss in liver transplant patients. Arterial complications, of which hepatic arterial thrombosis (HAT) is the most common, account for 64% to 82% of the vascular complications encountered (Bell et al, 1990; Leonardi et al, 2004). The overall incidence of HAT is 1.6% to 8% in various adult series, but it can be 15% to 26% in pediatric patients (Busuttil et al, 1991; Mazzaferro et al, 1989; Tan et al, 1988). The incidence of HAT in LDLT varies widely and is influenced by the type of graft, surgeon experience, and donor anatomy.

Doppler ultrasound (US) is the best screening method and should be used liberally in the first 2 weeks after transplantation with any change in graft function or significant elevation in bilirubin or transaminases. Because collateral blood flow through the gastroduodenal artery can result in a false-negative result, care must be taken to establish arterial flow within the hepatic parenchyma. In cases of suspected HAT revealed by US, confirmation should be made by celiac arteriography (Fig. 100.1) or multiphase computed tomography (CT). Failure to make a rapid diagnosis can result in hepatic necrosis and graft loss.

FIGURE 100.1 Hepatic artery thrombosis. The patient developed a rapid increase in serum transaminases in the early postoperative period. Ultrasound could not locate an intrahepatic arterial signal. Celiac arteriography shows left gastric and splenic arterial flow and fails to show any contrast in the liver. This is consistent with intimal dissection of the entire common hepatic artery. The T-tube within the common bile duct is visible.

Intimal dissection of the recipient hepatic artery down to the origin of the celiac axis is a common cause of intraoperative HAT. In these cases, immediate reconstruction with a donor iliac allograft is indicated (Fig. 100.2). Under no circumstances should the patient leave the operating room without a completely revascularized graft. When a donor iliac allograft is unusable or unavailable, an autogenous saphenous vein graft should be used. Rarely, an artificial conduit made from Dacron or expanded polytetrafluoroethylene can be used.

FIGURE 100.2 Hepatic artery reconstruction. With early diagnosis of hepatic artery thrombosis, immediate reconstruction with a donor iliac artery allograft can be performed. In this case, the iliac artery graft is anastomosed between the infrarenal aorta and liver allograft common hepatic artery.

The clinical presentation of HAT observed postoperatively ranges from a completely asymptomatic patient with minimal alterations in liver function to a critically ill patient with fulminant hepatic necrosis. A more common presentation of HAT is with postoperative biliary complications, including leaks and stricture formation (Margarit et al, 1998; Orons et al, 1995). Treatment for HAT in the early postoperative period is the same, whether symptoms are present or not: rapid reestablishment of arterial inflow should be attempted, which generally requires urgent operation with arterial reconstruction using a donor iliac artery allograft or autogenous graft material. Some authors have attempted thrombolysis using tissue plasminogen activator and urokinase, but this can be expected to be successful only when no technical factors are contributing to the thrombosis (Hidalgo et al, 1989). Hepatic artery intimal dissection is not amenable to thrombolytic therapy, and attempts at systemic thrombolysis waste valuable time and resources and worsen outcome. In most cases, 50% to 70% of patients ultimately require retransplantation (Langnas et al, 1991).

Portal Vein Thrombosis

PVT observed prior to surgery was previously considered an absolute contraindication to orthotopic liver transplantation (OLT). Although this problem no longer precludes successful liver transplantation, its presence may substantially increase the surgical complexity and perioperative morbidity.

Reconstitution of portal flow usually can be obtained through portal vein thrombectomy in most cases or by using a donor iliac vein allograft anastomosed between the superior mesenteric vein and liver allograft portal vein (Davidson et al, 1994; Shaked & Busuttil, 1991). Living-donor grafts that have relatively short portal vein segments can be difficult to reconstruct, and approximately 10% of institutions consider PVT an absolute contraindication to LDLT (Kadry et al, 2002).

PVT observed after transplantation is a rare complication that can occur in the immediate postoperative period, usually for technical reasons, such as incomplete thrombectomy or twisting of the anastomosis. PVT observed several months to years after transplantation usually results from intimal hyperplasia with gradual cavernous transformation with collaterals. A high index of suspicion is needed to make the diagnosis. Accumulation of ascites, splenomegaly, or the presence of varices after transplantation should prompt investigation. Early thrombosis is best treated with reoperation, thrombectomy, and systemic coagulation. The treatment of late thrombosis is more controversial, because direct repair is difficult. Transhepatic angioplasty with the placement of metal stents has been successful in some patients, whereas other patients have responded to selective shunting procedures to control variceal hemorrhage in the setting of adequate liver function (Jenkins et al, 1999; Raby et al, 1991).

Inferior Vena Cava Obstruction

Inferior vena cava (IVC) obstruction is a rare complication that occurs in 1% to 2% of patients after liver transplantation (Wozney et al, 1986). Most surgeons prefer to anastomose the donor IVC to the suprahepatic and infrahepatic IVC. A growing trend is to perform a so-called piggyback transplantation, with the anastomosis of the donor suprahepatic IVC to the confluence of the recipient middle and left hepatic veins, leaving the recipient IVC in situ (Neuhaus & Platz, 1994; Tzakis et al, 1989).

In our experience in 90 consecutive liver transplantations using the piggyback technique, two patients developed thrombus in their native IVC. The first IVC thrombosis developed in a patient with Budd-Chiari syndrome, who had occluded middle and left hepatic veins and a misplaced TIPS in the right hepatic vein that extended into the IVC at the time of transplantation. Postoperatively, the patient developed profound pedal edema and ascites. US confirmed the diagnosis, and the condition was treated successfully with anticoagulation and balloon dilation without further surgery. The second patient was a young man who was urgently transplanted for fulminant liver failure secondary to hepatitis A. Complicating this operation was the presence of a high-grade bacteremia with Staphylococcus aureus at the time of transplantation. Postoperatively, the patient did well but developed persistent fevers of an unknown source. Gallium scanning ultimately disclosed a nearly occluding infected thrombus in the infrarenal IVC. This thrombus was treated with long-term antibiotics and systemic anticoagulation with complete resolution after 6 weeks of therapy.

Treatment of an IVC thrombosis usually depends on the cause. Direct surgical removal is difficult in a critically ill patient and requires extensive mobilization of the right colon and small bowel mesentery to facilitate exposure. Medical management of IVC thrombosis was successful in our experience and that reported by others (Kraus et al, 1992). Our experience suggests that a more conservative management algorithm that employs invasive radiologic procedures and systemic anticoagulation can treat this complication satisfactorily (Kraus et al, 1992). Thrombolytic therapy can also be adjunctive in resolving “fresh” thrombus formation.

Biliary Leaks

The reported incidence of biliary leaks after liver transplantation varies widely from 10% to 50% (Rabkin et al, 1998; Reichert et al, 1998). Leaks are observed most commonly at the site of choledochal anastomosis or the choledochal T-tube insertion site. Leaks at the choledochal tube insertion site are observed most commonly at the time of tube removal and occur in 25% to 40% of patients (O’Connor et al, 1995). Most of these patients can be managed conservatively with a short course of analgesics and antibiotics. To minimize this risk, some surgeons prefer not to place stents.

In our practice, rather than using a conventional T-tube, we stent our choledochal anastomosis with a 5-Fr pediatric feeding tube placed through the cystic duct stump, which is secured with a hemorrhoidal band and polydioxanone suture (PDS). In theory, the hemorrhoidal band obliterates the lumen of the preformed tract at the time of stent removal, usually 6 to 8 weeks postoperatively. Anastomotic leaks encountered in the early postoperative period are related to technical errors, tension at the anastomotic site, or ischemic necrosis after hepatic artery thrombosis.

The bile ducts of living-donor or split-liver grafts can be reconstructed with a duct-to-duct (choledochocholedochostomy) or Roux-en-Y hepaticojejunostomy. The leak rate is similar with both types of reconstructions (Gondolesi et al, 2004). Signs and symptoms related to biliary leaks include bilious fluid in drains (biliary fistula), abdominal or shoulder pain or both, increased serum bilirubin, nausea, vomiting, and fever. Diagnosis can be confirmed by cholangiography if a choledochal tube is in place; otherwise, endoscopic retrograde cholangiography (ERC) or percutaneous transhepatic cholangiography (PTC) can be performed. We favor ERC, because treatment with endoscopic stent placement can be readily achieved without the risk associated with the indwelling transhepatic catheters used during PTC. Large biliary leaks resulting in bile collections adjacent to the liver require percutaneous drainage.

Leaks associated with ischemic necrosis require surgical revision with Roux-en-Y hepaticojejunostomy. The development of early postoperative leaks is associated with late stricture formation, and lifelong surveillance by the surgeon is warranted.

Biliary Stricture or Obstruction

Biliary obstruction occurs in approximately 7% to 15% of patients after liver transplantation (Klein et al, 1991; Lerut et al, 1987). As with leaks, the site of obstruction aids in determining the cause. Anastomotic stricture accounts for 50% of obstruction cases and can occur early in the postoperative period, secondary to edema, or later, as a result of compromised blood supply (Fig. 100.3). Biliary strictures usually present within weeks but may occur years after transplantation. Two types of biliary obstruction usually are found: anastomotic and nonanastomotic. Nonanastomotic obstruction or stricture can be caused by or associated with bile duct ischemia or sludge and debris that can accumulate in the biliary system after transplanting (Fig. 100.4).

FIGURE 100.3 Biliary stricture. This patient had a previously created Roux-en-Y hepaticojejunostomy and now has an anastomotic stricture. Note the dilated intrahepatic ducts. Percutaneous access of the Roux-en-Y limb affords the ability to make the diagnosis and treat with balloon dilation. Using this technique, placement of transhepatic catheters is avoided.

FIGURE 100.4 Nonanastomotic biliary stricture observed from ischemic injury to a liver graft in a patient who received a liver from a donor who died from cardiac death rather than brain death. Donation after cardiac death (DCD), rather than after brain death, is an attempt to expand the organ donor pool; but such grafts are more prone to ischemic injury problems such as bile duct stricture.